A novel signature mutation for oxidative damage resembles a mutational pattern found commonly in human cancers

Mitchell S. Turker, Blythe M. Gage, Jennifer A. Rose, Daniel Elroy, Olga N. Ponomareva, Peter J. Stambrook, Jay A. Tischfield

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

To determine the types of mutations induced by oxidative damage, a kidney cell line with a heterozygous deficiency for the autosomal Aprt (adenine phosphoribosyltransferase) gene was tested for its mutagenic response to hydrogen peroxide. Aprt-deficient cells were selected and scored for loss of heterozygosity (LOH) for 11 microsatellite loci on mouse chromosome 8. On the basis of the LOH analysis, spontaneous mutants (n = 38) were distributed into four classes: apparent point mutation, mitotic recombination, chromosome loss, and large interstitial deletion. However, 9 of 20 (45%) hydrogen peroxide-induced mutants exhibited a novel class of mutations characterized by 'discontinuous LOH' for one or more of the microsatellite loci. Interestingly, mutations resembling discontinuous LOH are commonly observed in a wide variety of human cancers. Our data suggest that discontinuous LOH is a signature mutational pattern for oxidative damage and further suggest that such genetic damage is widespread in cancer.

Original languageEnglish (US)
Pages (from-to)1837-1839
Number of pages3
JournalCancer Research
Volume59
Issue number8
StatePublished - Apr 15 1999

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Turker, M. S., Gage, B. M., Rose, J. A., Elroy, D., Ponomareva, O. N., Stambrook, P. J., & Tischfield, J. A. (1999). A novel signature mutation for oxidative damage resembles a mutational pattern found commonly in human cancers. Cancer Research, 59(8), 1837-1839.